ABSTRACT:
Understanding
the role of neurotransmission in the prefrontal cortex and mesolimbic brain regions
has become the subject of intensive neuroscience research worldwide. In the
1970s, our group provided evidences that rats exposed to darkness significantly
augmented their alcohol intake. At that time, we proposed that melatonin was
the culprit. At around the same time, our laboratory, amongst a few others,
proposed that dopamine-adducts with acetaldehyde to induce alcohol intake both
in rodents and in humans. While the work in these areas has declined considerably
over the years, more recent scientifically sound studies continue to show the
importance of these earlier controversial ideas involving alcohol abuse and
alcoholism. A review of the literature has provided impetus to systematically
access the newer genetic and molecular neurobiological findings relevant to the
physiological and psychological motives for high alcohol consumption in animals
and humans alike. Thus, we hypothesize that darkness-induced alcohol intake is
linked not only to serotonergic-melatonin mechanisms, but also to dopaminergic
regulation of brain mesolimbic pathways involving neuronal expression switching
in response to long photoperiods affecting gene expression.